Excerpt:

Conclusions and Perspectives

The results obtained so far on the cellular mechanism by which fluoride may influence the growth and differentiation of osteoblastic cell lines strongly suggest alteration of one or several G protein-dependent tyrosine phosphorylation process(es), activation of the ERK, and possibly other signaling pathways. There is a controversy of whether enhancement of tyrosine phosphorylation induced by fluoride results from inhibition of tyrosine phosphatase(s) or activation of tyrosine kinase(s), and evidence for either mechanism has been presented in this mini-review. For both working hypotheses, further investigation is required to determine the molecular target(s) responsible for inducing the alteration in tyrosine phosphorylation and enhancement of cell proliferation.

Despite the fact that the clinical application of fluoride in the treatment of osteoporosis remains controversial, the elucidation of its action mechanism at the molecular level will certainly provide useful information for the development of new pharmacological agents able to enhance osteoblastic proliferation and ultimately correct the deficit of bone mass and strength in osteoporosis.

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